The purpose of the proposed study is to test the hypothesis that psychological factors, operationalized as an acute laboratory stressor, influence immunologic mediators of airway inflammation in adolescents with atopic asthma. This knowledge will improve our understanding of the potential mechanisms linking psychological factors to physiological changes in asthma, and could serve to identify an additional subgroup of asthmatics who might benefit from psychological intervention to reduce stress. Research indicates that 20-25% of people with asthma experience stress-related bronchoconstriction that is hypothesized to be mediated by the autonomic nervous system. Despite the fact that underlying inflammation is a critical component of asthma, little is known about how stress influences inflammatory processes in asthma. Several immune mediators (i.e., cytokines) are known to regulate lung inflammation in asthma. The proposed research will show whether a change in cytokine production by T-helper type 1 (TH 1) or T-helper type 2 (TH2) cells in response to stress is one mechanism for the link between stress and asthma symptoms in some people. Eighty adolescents with atopic asthma and 40 healthy adolescents ages 14-18 will participate. Half of the subjects with asthma will have reported that stress or emotions is a trigger for their asthma symptoms. Each subject will participate in an 8-hour laboratory protocol. After placement of an IV catheter, subjects will be exposed to a stressor, operationalized as a standardized interview about a distressing event. Physiological and biochemical measures of autonomic reactivity will be obtained. Pulmonary function will be measured. Questionnaires about stressful life events will be completed. Blood samples drawn at 7 discrete time periods up to 7 hours after the beginning of the stressor will be analyzed for the presence of cytokines (e.g., interleukin-4, interleukin-5, interferon-gamma) that are involved in inflammatory processes in asthma. Enumerative (e.g., percentages of lymphocytes producing TH1 vs. TH2 cytokines) and functional (e.g., relative concentrations of TH1 vs. TH2 cytokines) methods will be used. It is expected that: 1. Adolescents with asthma will exhibit a greater stress-induced shift toward a TH2 immune response than healthy controls, and, 2. The degree of shift toward a TH2 immune response will correlate with psychophysiological indices of stress. Techniques of analysis of variance with repeated measures and multiple regression will be used. Results will further our knowledge of the relationships between stress and immunity in asthma.